Oxidative stress and hepatitis C virus

Abstract

The disproportionate imbalance between the systemic manifestation of reactive oxygen species and body’s ability to detoxify the reactive intermediates is referred to as oxidative stress. Several biological processes as well as infectious agents, physiological or environmental stress, and perturbed antioxidant response can promote oxidative stress. Oxidative stress usually happens when cells are exposed to more electrically charged reactive oxygen species (ROS) such as H2O2 or O2-. The cells’ ability to handle such pro-oxidant species is impeded by viral infections particularly within liver that plays an important role in metabolism and detoxification of harmful substances. During liver diseases (such as hepatocellular or cholestatic problems), the produced ROS are involved in transcriptional activation of a large number of cytokines and growth factors, and continued production of ROS and Reactive Nitrogen Species (RNS) feed into the vicious cycle. Many human viruses like HCV are evolved to manipulate this delicate pro- and antioxidant balance; thus generating the sustainable oxidative stress that not only causes hepatic damage but also stimulates the processes to reduce treatment of damage. In this review article, the oxidant and antioxidant pathways that are perturbed by HCV genes are discussed. In the first line of risk, the pathways of lipid metabolism present a clear danger in accumulation of viral induced ROS. Viral infection leads to decrease in cellular concentrations of glutathione (GSH) resulting in oxidation of important components of cells such as proteins, DNA and lipids as well as double strand breakage of DNA. These disorders have the tendency to lead the cells toward cirrhosis and hepatocellular carcinoma in adults due to constant insult. We have highlighted the importance of such pathways and revealed differences in the extent of oxidative stress caused by HCV infection.

Serum total antioxidant capacity status of HTLV-1 infected patients

“…Several studies have highlighted the oxidative stress in some chronic viral infections (Oliveira et al, 2011;Paracha et al, 2013;Zhao et al, 2013), and different mechanisms for such oxidative stress have been suggested. In HIV, for example, decreased antioxidant defense and/or elevated serum levels of lipid peroxidation byproducts have been proposed (Dworkin et al, 1986;Sonnerborg et al, 1988;Revillard et al, 1992;Coodley et al, 1993;Dworkin, 1994;Favier et al, 1994;Akerlund, 1994 Schrauzer andSacher, 1994).…”

“…Total antioxidant capacity is a marker of antioxidant status, which may serve as an indicator of oxidant/antioxidant imbalance (Suresh et al, 2009). Different studies have addressed oxidative stress in malignancies (Rahal et al, 2014), inflammatory conditions including autoimmune diseases (Kundu et al, 2012;Norheim et al, 2012;Wakamatsu et al, 2013), as well as chronic infections such as HIV-1 (Oliveira et al, 2011), HBV (Zhao et al, 2013), and HCV (Paracha et al, 2013).…”

Grape seed protects cholestatic rats liver from ischemia/reperfusion injury

“…Therefore, the tissue GSH level has been accepted as a marker for oxidative stress injury. Less tissue GSH level means more oxidative stress injury 21 . In our study, GSE treatment provides attenuation of oxidative stress injury in a cholestatic I/R injury model.…”

Oxidative Stress Attenuates Lipid Synthesis and Increases Mitochondrial Fatty Acid Oxidation in Hepatoma Cells Infected with Hepatitis C Virus

“…Oxidative/nitrosative stress essentially arises when the production of reactive oxygen (and nitrogen) species (ROS and RNS, respectively) exceeds cellular antioxidant defenses. HCV-induced oxidative/nitrosative stress has been observed in vivo and in vitro (5)(6)(7)(8)(9) and has been assigned to almost all HCV proteins (i.e. core, E1, E2, NS3/4A, NS4B, and NS5A) (5), with core being the most potent inducer (10,11).…”

“…The cellular mechanisms by which HCV replication might mediate liver injury are unclear, but there is no doubt that oxidative/nitrosative stress in HCV-infected cells plays an important role in the initiation and progression of liver damage (3,5,6). Oxidative/nitrosative stress essentially arises when the production of reactive oxygen (and nitrogen) species (ROS and RNS, respectively) exceeds cellular antioxidant defenses.…”